Effect of hydrostatic pressure on ADH induced osmotic water flow in toad bladder.
The effect of hydrostatic pressure (HP) on antidiuretic hormone (ADH) stimulated osmotic water flow (Jv) across the toad urinary bladder was evaluated. Jv for ADH-stimulated bladders was significantly reduced by an elevation of the serosal HP gradient to 1 cm H2O. Subsequent elimination of the HP gradient resulted in a recovery of Jv. Serosal HP also caused a reversible increase in sucrose permeability (P sucrose). For ADH-treated bladders fixed with glutaraldehyde during serosal HP exposure, subsequent exposure to a mucosal or serosal HP gradient caused acceleration or inhibition of Jv, respectively. The reduction in ADH-associated Jv with serosal HP was apparently caused by a back-flux of water through a paracellular pathway. Jv and P sucrose were not affected by mucosal HP during ADH stimulation. The results suggest a specific sensitivity of a paracellular pathway to a small serosal HP gradient in bladders with ADH-stimulated water flow. The reversibility of this effect on P sucrose suggests that the elements comprising the apical junctions are dynamic structures capable of recovering at least some of their permeability properties.
D000818:Animals; D001692:Biological Transport; D002024:Bufo marinus; D004848:Epithelium / Q000378:metabolism; D005260:Female; D006874:Hydrostatic Pressure; D009995:Osmosis; D010539:Permeability; D011312:Pressure; D013395:Sucrose / Q000378:metabolism; D001743:Urinary Bladder / Q000378:metabolism*; D014667:Vasopressins / Q000494:pharmacology*; D014867:Water / Q000378:metabolism*
D014867:Water; D014667:Vasopressins; D013395:Sucrose